PRKAG3 polymorphisms associated with sporadic Wolff-Parkinson-White syndrome among a Taiwanese population.

BACKGROUND: The aim of this study was to investigate whether mutation in AMP-activated protein kinase (AMPK) subunit genes (PRKAG3-230) is associated with sporadic, isolated Wolff-Parkinson-White (WPW) syndrome. METHODS: This study consisted of 87 patients with symptomatic WPW syndrome and 93 healthy controls. PRKAG3-230 genotypes were determined using real-time polymerase chain reaction assay. Genotype and allele frequencies of PRKAG3-230 between patients with WPW syndrome and healthy controls were ascertained using chi-square test or Fisher exact test when appropriate. RESULTS: PRKAG3-230 were genotyped in 87 patients (53 men and 34 women; age=24.4±18.0 years) with WPW syndrome and 93 healthy controls (57 men and 36 women; age=16.8±4.2 years). There were no significant differences between the two groups in terms of age and sex. The patients with CG and CG+CC genotypes had a significantly increased risk of WPW syndrome compared with those with GG genotype [odds ratio (OR)=1.99, 95% confidence interval (CI)=1.01-3.89, p=0.045; OR=1.99, 95% CI=1.04-3.78, p=0.037, respectively]. The allelic types were not associated with the risk of WPW syndrome. The patients with manifest type with CG and CG+CC genotypes had a significantly increased risk of WPW syndrome compared with those with GG genotype (OR=2.86, 95% CI=1.16-7.05, p=0.022; OR=2.84, 95% CI=1.19-6.80, p=0.019, respectively). The patients with right-side accessory pathways with CG and CG+CC genotypes had a significantly increased risk of WPW syndrome compared with those with GG genotype (OR=3.07, 95% CI=1.25-7.51, p=0.014; OR=2.84, 95% CI=1.19-6.80, p=0.019, respectively). The allelic types were not associated with the risk of WPW types and locations. CONCLUSION: This study shows that PRKAG3-230 may be associated with sporadic WPW syndrome among a Taiwanese population. Further studies are warranted to elucidate the role of mutations in AMPK subunit genes other than PRKAG3-230 in sporadic WPW syndrome.

Long-Term Prognosis in Recipients of Implantable Cardioverter-Defibrillators for Secondary Preventions in Taiwan - A Multicenter Registry Study.

BACKGROUND: The use of an implantable cardioverter-defibrillator (ICD) has a proven capacity to prevent sudden cardiac death (SCD), and can also improve survival duration in well-selected patients. The goal of the present study was to investigate the long-term prognosis and predictors of mortalities among ICD recipients in Taiwan. METHODS: From 1998 to 2009, 238 consecutive patients who experienced SCDs or life-threatening ventricular tachyarrhythmias without correctable causes and received ICD implantations in 3 medical centers (Taipei, Taichung and Kaohsiung Veterans General Hospital) were enrolled in this study. The clinical endpoint was defined as the occurrence of all-cause mortality during the follow-up. RESULTS: The mean age of the patients was 63.0 ± 15.3 years, and 76.5% of them were male. Ischemic cardiomyopathy was the leading cause for the ICD implantations (39.1%). During the mean follow-up duration of 36.8 ± 29.8 months, there were 48 patients (20.2%) who died. Patients with structural heart diseases had a higher mortality rate than those without such diseases. Additionally, old age, low left ventricular ejection fraction (LVEF) and a history of diabetes mellitus (DM) were significant predictors of mortality. The optimal cutoff values for age (70 years) and LVEF (40%) in predicting mortality were further identified using the receiver operating characteristic curves. CONCLUSIONS: Based on the ICD registry from 3 medical centers in Taiwan, the annual mortality rate was around 6.6% and was higher in those patients with structural heart diseases. We observed that old age, low LVEF and a history of DM were significant predictors of mortality. KEY WORDS: Implantable cardioverter-defibrillator; Mortality; Predictor; Taiwan.

The Effect of Intensified Low Density Lipoprotein Cholesterol Reduction on Recurrent Myocardial Infarction and Cardiovascular Mortality.

BACKGROUND: Lipid-lowering therapy plays an important role in preventing the recurrence of cardiovascular events in patients after acute myocardial infarction (AMI). This study aimed to assess the effect of intensified low density lipoprotein cholesterol (LDL-C) reduction on recurrent myocardial infarction and cardiovascular mortality in patients after AMI. METHOD: The 562 enrolled AMI patients (84.2% male) were divided into two groups according to 3-month LDL-C decrease percentage equal to or more than 40% (n = 165) and less than 40% (n = 397). To evaluate the long-term efficacy of LDL-C reduction, the 5-year outcomes were collected, including time to the first occurrence of myocardial infarction and time to cardiovascular death. RESULTS: The baseline characteristics and complication rates were not different between the two study groups. The patients with 3-month LDL-C decrease ≥ 40% had higher baseline LDL-C and lower 3-month, 1-year, 2-year, 3-year, 4-year and 5-year LDL-C than the patients with 3-month LDL-C decrease < 40%. In Kaplan-Meier analyses, those patients with 3-month LDL-C decrease ≥ 40% had a higher rate of freedom from myocardial infarction (p = 0.006) and survival rate (p = 0.02) at 5-year follow-up. The 3-month LDL-C < 40% parameter was significantly related to cardiovascular death (HR: 9.62, 95% CI 1.18-78.62, p < 0.04). CONCLUSIONS: After acute myocardial infarction, 3-month LDL-C decrease < 40% was identified to be a significant risk factor for predicting 5-year cardiovascular death. The patients with 3-month LDL-C decrease ≥ 40% had a higher rate of freedom from myocardial infarction and lower cardiovascular mortality, even though these patients had higher baseline LDL-C value. KEY WORDS: Acute myocardial infarction; Cardiovascular death; Low-density lipoprotein cholesterol; Mortality; Statin.

Recurrent syncope due to carotid sinus hypersensitivity and sick sinus syndrome.

Syncope is a sudden and brief loss of consciousness with postural tone. Its recovery is usually spontaneous. There are various causes of syncope including cardiac, vascular, neurologic, metabolic and miscellaneous origins. The tracing is usually time-consuming and costly. The diagnosis of carotid sinus syncope may sometimes be difficult since the symptoms are nonspecific, especially in older persons. Here, we report the case of a 72-year-old woman who sought medical attention at our hospital due to repeated syncope episodes over the previous 5 years. Neurologic examinations showed negative results (including brain computed tomography). Twenty-four-hour ambulatory electrocardiogram monitoring showed atrial and ventricular premature contractions only. Electrophysiologic study disclosed prolonged corrected sinus node recovery time (1,737 ms) with poor atrioventricular conduction. Drop of blood pressure together with sinus bradycardia developed after left side carotid sinus massage. Both carotid sinus hypersensitivity with sick sinus syndrome contributed to this patient's syncope, and after pacemaker placement together with selective serotonin reuptake inhibitor treatment, she was free from syncope thereafter.

Assessing culprit lesions and active complex lesions in patients with early acute myocardial infarction by multidetector computed tomography.

BACKGROUND: Accurate, non-invasive characterization of culprit lesions in patients after acute myocardial infarction (AMI) remains challenging. In this prospective study, multidetector row computed tomography (MDCT) is used to assess culprit and active complex lesions in patients early after AMI. METHODS AND RESULTS: We enrolled 103 patients with first non ST-elevation AMI who underwent 64-slices MDCT and conventional coronary angiography (CCAG). The definition of culprit lesion, stable non-culprit lesions and non-culprit active complex lesions was based on the findings of CCAG. The lesions were analyzed with MDCT data. In culprit lesions (n=103), luminal artery stenosis, remodeling index, plaque area and burden were significantly higher than non-culprit lesions (n=129). Multivariate discriminant analysis showed that MDCT density could discriminate culprit from non-culprit lesions. Receiver-operator characteristic curve analysis identified the optimal cutoff value of lesion density for discrimination between culprit and non-culprit lesion as 49.6 Hounsfield units (HU); this value was associated with a sensitivity, specificity and accuracy of 88.4%, 87.4%, and 87.9%, respectively. The MDCT in the stable non-culprit lesions (81.8+/-15.5 HU) was significantly higher than that in culprit lesions or non-culprit active complex lesions (33.2+/-13.8 and 48.3+/-15.7 HU, p<0.001). CONCLUSIONS: MDCT can predict culprit lesions in patients early after AMI, and identify multiple complex lesions.

Role of shortened QTc dispersion in in-hospital cardiac events in patients undergoing percutaneous coronary intervention for acute coronary syndrome.

BACKGROUND: QT dispersion (QTD) refers to the difference between maximal and minimal QT values on the electrocardiogram (ECG). QTD values are calculated and corrected with Bazett's formula (corrected QTD = QTcD = QTD/square root of RR). QTcD increases in patients with acute coronary syndrome (ACS). Recovery of increased QTcD (shortened QTcD) develops after successful revascularization, but prolonged QTcD occurs in certain patients. The aim of this study is to ascertain the clinical significance between shortened and prolonged QTcD groups after percutaneous coronary intervention (PCI). METHODS: We retrospectively enrolled 128 patients with ACS who had received PCI. The values of QTcD were measured manually on 12-lead standard ECGs obtained within 3 days before and after PCI (pre-PCI QTcD and post-PCI QTcD). All the patients were divided into 2 groups. The shortened QTcD group was defined as those patients with a decrease in QTcD after PCI and the prolonged QTcD group as those with an increase in QTcD after PCI. The underlying diseases, various clinical classifications and some prognostic factors were taken into comparison and statistical analysis between these 2 groups. RESULTS: The shortened QTcD group showed a significantly higher rate of in-hospital cardiac death (13% vs. 0%, p = 0.006) and a greater pre-PCI QTcD (100.8 +/- 39.5 vs. 61.3 +/- 24.1 ms, p < 0.001) than the prolonged QTcD group. There was a significantly greater pre-PCI QTcD in patients with cardiac death than those without cardiac death (111.6 +/- 38.3 vs. 83.3 +/- 38.3ms, p = 0.027). Furthermore, the patients with in-hospital cardiac death presented with a significantly more frequent occurrence of in-hospital ventricular arrhythmia, compared with those without cardiac death (30.0% vs. 4.0%, p = 0.014). CONCLUSION: Among the patients with ACS undergoing PCI, directly divided into shortened and prolonged QTcD groups regardless of initial pre-PCI QTcD, the shortened QTcD group showed a higher occurrence of in-hospital cardiac death and a greater pre-PCI QTcD. Shortened QTcD might be 1 risk factor for in-hospital cardiac death.

Acute effects of dual-chamber pacing on the left ventricular systolic function and relaxation in patients with advanced AV block and sick sinus syndrome.

BACKGROUND: Abnormal activation of the ventricles via right ventricular apical pacing deteriorates cardiac function, which may explain the increased mortality of patients with congestive heart failure receiving permanent pacemakers. We hypothesized that pacing at alternative sites may cause less detrimental effects on the cardiac function. METHODS: Five symptomatic patients with either advanced AV block (n = 4) or sick sinus syndrome with normal left ventricular (LV) function (n = 1) were studied. During cardiac catheterization, LV pressure was recorded with a high-fidelity catheter-tipped transducer. Baseline rhythms were sinus rhythm or VVI pacing. Sequential VDD pacing with variable AV intervals was performed at the right ventricular apex (RVA), right ventricular septum (RVS), right ventricular outflow tract (RVOT) and coronary sinus (CS). LV systolic function was assessed by calculating dP/dt(max) and LV diastolic function was indexed by calculating the exponential isovolumic relaxation constant (Tau). Percentage changes (mean +/- SE) from baseline to pacing were measured. RESULTS: RVA pacing reduced dP/dt(max) (-0.8 +/- 8.4%) and prolonged Tau (7.0 +/- 5.6%); RVS pacing enhanced dP/dt(max) (20.7 +/- 15.3%) and shortened Tau (-10.4 +/- 9%); RVOT pacing reduced dP/dt(max) (-8.0 +/- 20.0%) and shortened Tau (-6.0 +/- 12.2%); CS pacing reduced dP/dt(max) (-11.7 +/- 13.0%) and prolonged Tau (10.5 +/- 11.9%). Our results demonstrated that different pacing sites have different effects on LV contractility and relaxation in patients with normal LV function. CONCLUSION: Since pacing at the RVS preferably increased LV dP/dt(max) and shortened Tau, it may be a better alternative than the RVA.